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Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes. RNA was extracted from livers, spleens and brains of 7-9 week old male C57Bl/6 mice infected with gammaherpesvirus 68 (MHV68), a virus defective in establishment of latency (ORF73.stop) or mockulum. RNA from 3-4 mice per treatment was pooled and analyzed by M430 2.0 Affymetrix Gene Chip. Three biologic replicates were analyzed for all conditions, except mock livers, for which four biologic replicates were analyzed.
2013-10-18 | E-GEOD-51365 | biostudies-arrayexpress
Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes.
2013-10-18 | GSE51365 | GEO
Project description:Vero cells were infected with Zika virus in three biological replicates and sampled at three post-infection timepoints (12 hrs, 24 hrs, 48 hrs). Biological replicate mock uninfected cells were also done for each timepoint. We used TMT6 labeled quantitation at each timepoint to examine proteome changes in response to infection.
2020-03-05 | MSV000085057 | MassIVE
Project description:Objective: Multiple sclerosis (MS) is a chronic, autoimmune disease of the central nervous system. Prior infection with Epstein-Barr virus (EBV), a gammaherpesvirus, is deemed a necessary yet insufficient factor in the development of MS. The objective of this study was to determine whether the EBV-like virus, murid gammaherpesvirus 68, is sufficient to induce inflammatory demyelinating disease in a transgenic TCR mouse strain susceptible to CNS autoimmunity. Methods: B10.PL mice that express the myelin basic protein-specific transgenic T cell receptor (TCRMBP) were intranasally inoculated with murid gammaherpesvirus 68 virus (MHV68), PR8 influenza virus, or PBS. Mice were evaluated for the development of neurologic deficits. Flow cytometry and fluorescent microscopy were used to validate the infiltration of immune cells in the brain and spinal cord of TCRMBP mice. Single cell RNA sequencing of splenic B cells was performed to determine transcriptional changes that resulted from MHV68 infection. Results: MHV68-infected mice developed neurological deficits at a significantly higher frequency (70.8%) than the influenza (7.7%) or mock-infected mice (13.3%). MHV68 infected mice exhibited signs including optic neuritis and ataxia, which are infrequently observed in EAE mice, but common in MS patients. MHV68-infected mice exhibited increased focal immune cell infiltration. Single cell RNA sequencing identified the emergence of a novel, MHV68 infection-associated population of memory-like B cells that highly express genes associated with antigen presentation and costimulation. Conclusion: Infecting myelin basic protein specific TCR transgenic mice with the EBV analogue, MHV68, generates encephalitogenic disease without myelin immunization. MHV68 drives a distinct transcriptional program in B cells capable of enhanced antigen presentation and costimulation to drive an autoreactive T cell response.
2024-04-02 | GSE261605 | GEO
Project description:Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease. We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes. Early passage primary endothelial cells (HUVECs) were mock infected (no virus) or infected with dengue virus and total RNA collected at 3 timepoints: 12, 24, and 48 hours post infection. Multiple timepoints were analyzed to identify changes in gene expression levels over time. Gene expression from both mock infected and dengue virus infected endothelial cells was evaluated to determine fold induction at each timepoint.
2012-04-10 | E-GEOD-34628 | biostudies-arrayexpress
Project description:MHV68 ORF50stop Vaccine Gene Expression
| PRJNA945888 | ENA
Project description:Ribosome profiling (RiboSeq) (maps positions of translating ribosomes on the transcriptome) and RNASeq (quantifies the transcriptome) analysis of murine L929 cells infected with encephalomyocarditis virus vMC0. Samples comprise 2, 4, 6 and 8 h post infection RiboSeq timecourses for WT virus and a shift mutant [SS] (8 samples), and RiboSeq and RNASeq at 8 h post infection for WT virus and 5 mutant viruses (shift site [SS], stem-loop [WT-SL], shift site and stem-loop [SS-SL], StopGo [LV], and StopGo, shift site and stem-loop [LV-SS-SL]) (12 samples).
2017-06-02 | E-MTAB-5206 | biostudies-arrayexpress
Project description:We infected bone marrow derived macrophages (BMDM) with wild type vaccinia virus Western Reserve (WT-WR) and mutant virus deleting A26 protein (WRΔA26) and analyzed transcriptional profiling of cellular genes at 1, 2, 4 and 8 hours post-infection times (p.i.).
2017-07-09 | GSE97705 | GEO
Project description:MicroRNA (miRNA) and endogenous siRNA (endo-siRNA) are two essential classes of small noncoding RNAs (sncRNAs) in eukaryotic organisms. The class of miRNA is diverse and there exist noncanonical miRNAs that bypass the canonical miRNA biogenesis pathway. In order to identify noncanonical miRNAs and endo-siRNAs responding to virus infection and study their potential function, we sequenced small-RNA species from cells lytically infected with murine gammaherpesvirus 68. In addition to 3 novel canonical miRNAs in mouse, two antisense miRNAs in virus and 25 novel noncanonical miRNAs, including miRNAs derived from tRNAs, snoRNAs and introns, in the host were identified. These noncanonical miRNAs exhibited features distinct from canonical miRNAs in the lengths and structures of miRNA hairpins as well as base pairings and first nucleotide preference. Many of the novel miRNAs are conserved in mammals. In addition to several known murine endo-siRNAs detected by the sequencing profiling, a novel locus in the mouse genome was identified to give rise to endo-siRNAs. This novel endo-siRNA locus is comprised of two tandem inverted B4 short interspersed nuclear elements (SINEs). Unexpectedly, the SINE-derived endo-siRNAs were found in a variety of sequencing data as well as virus-infected cells. Moreover, a murine miRNA was up-regulated more than 35 fold in infected than in mock-treated cells. The putative target genes of the viral and the up-regulated murine miRNAs were potentially involved in processes of gene transcription and protein phosphorylation and localized to membranes, suggesting their role in manipulating the host basal immune system during lytic infection. Our results extended the number of noncanonical miRNAs in mammals and shed new lights on their potential functions of lytic infection of MHV68. Mouse NIH 3T12 cells infectd with MHV68 (3 samples) and mock-treated (2 samples) were examined. Noncanonical microRNAs and endogenous siRNAs discovery in lytic infection of murine gammaherpesvirus MHV68 (NC_001826.2).
2012-12-31 | E-GEOD-36639 | biostudies-arrayexpress
Project description:Purpose of this experiment was to further understand how innate immune defenses impact host response and West Nile virus tissue tropism. This study examined host-transcriptional response to West Nile virus in permissive and nonpermissive tissues using wildtype mice and mice with genetically altered interferon signaling pathways. Age-matched six to twelve week old mice were inoculated subcutaneously in the left rear footpad with 100 PFU of West Nile virus isolate TX 2002-HC (WNV-TX) in a 10 microL inoculum diluted in Hanks balanced salt solution (HBSS) supplemented with 1% heat-inactivated FBS. Mice were monitored daily for morbidity and mortality. Expression oligonucleotide arrays were performed on RNA isolated from spleen and liver tissues from strain and time-matched mock infected mice (n=2) and WNV-TX infected wild type (WT; n=3; day 4 post-infection), Ips-1-/-(n=3; day 4 post-infection), Ifnar-/- (n=3; day 2 post-infection), and Ips-1-/-xIfnar-/- (DKO; n=3; day 4 post-infection) mice.
2012-12-19 | E-GEOD-39259 | biostudies-arrayexpress